Transient mutism after brain stem infarction (ref. Acta Neurochirurgia 1999, 141: 209-213)
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BACKGROUND AND PURPOSE: We studied six patients suffering from pure, unilateral brain stem infarction to explore the association of remote cerebral and cerebellar blood flow changes with damage at different sites of this region of the brain. METHODS: We used single-photon emission computed tomography and [123I]iodoamphetamine to measure regional differences in tracer uptake. Qualitative image analysis and calculated asymmetry indexes were correlated to the location of the infarcted area on magnetic resonance imaging and to the patients' clinical findings. RESULTS: Significant perfusion asymmetries were noted in the two patients with infarction in the upper pons but not in those with lesions below this level. They comprised a contralateral cerebellar and ipsilateral supratentorial hypoactivity that was most marked in the frontoparietal cortex. There was no clear relation between the patterns of cerebral or cerebellar tracer uptake and specific neurological findings. CONCLUSIONS: Remote perfusion changes after pure brain stem infarction may be seen both infratentorially and supratentorially and depend on the lesion site rather than on the neurological deficit. In this context, our study confirmed damage to the corticopontocerebellar pathways as the key event in the genesis of a crossed cerebellar diaschisis. The exact mechanisms causing ipsilateral cerebral hemispheric diaschisis await further clarification.
Studies with MRI and non-invasive vascular imaging have modified previous conceptions on clinical spectrum and causes of different types of brain stem infarcts. Wallenberg's syndrome caused by lateral medullary infarction (LMI) often presents with patterns of sensory loss different from the "classical" crossed type. LMI carries a risk for respiratory and cardiovascular complications in the acute phase, warranting close patient monitoring. Medial medullary infarcts often present with a lacunar syndrome mimicking capsular or pontine small vessel disease. Cerebellar infarcts are most often caused by cardiac embolism. Isolated vertigo may be the only presenting symptom. Neurosurgical intervention of expansive cerebellar infarcts may be life-saving. Clinical features of progressive multifocal brain-stem symptoms are often suggestive of basilar artery occlusion. CT-angiography is a useful initial diagnostic tool. Based on observational studies, intraarterial thrombolysis is used in selected patients with basilar artery occlusion, but further studies are needed to define treatment criteria more precisely.
Two cases of brain stem infarction as an early and fatal complication of giant-cell arteritis are reported. These complications occurred despite adequate treatment with corticosteroids. The findings at autopsy are compared with those of the literature. The possible pathogenetic mechanisms of vertebro basilar occlusion and the therapeutical implications are discussed.
A case of brain stem infarction after chiropractic manipulation of the cervical spine is presented. Proposed mechanisms and sites of possible arterial injury are discussed. A diagnosis of vertebral artery occlusion was made using conventional brachial angiography. Digital intravenous angiography, a relatively new and less invasive vascular imaging technique which was used as an adjunct for evaluating the remainder of the cervicocephalic vessels, documented the vertebral occlusion. Chiropractic manipulation, which is increasing in popularity, may be a cause of potentially devastating neurologic disease.
Two patients sustained an ischemic brain stem infarction during medical examination and treatment. The first patient lost consciousness and the spontaneous respiration ceased during X-ray examination of the cervical spine when the neck was hyperextended. After some minutes he regained conciousness but was found to be tetraplegic, and the patient deceased 4 months later. The angiogram revealed thrombosis of the basilar artery. The other patient had profuse nosebleed and was treated with posterior tamponation during which she sat for about 10 min with the neck hyperextended. Some hours after this procedure symptoms and signs of lateral caudal brain stem infarction emerged.
A case of brain stem infarction after chiropractic manipulation of the cervical spine is presented. Proposed mechanisms and sites of possible arterial injury are discussed. A diagnosis of vertebral artery occlusion was made using conventional brachial angiography. Digital intravenous angiography, a relatively new and less invasive vascular imaging technique which was used as an adjunct for evaluating the remainder of the cervicocephalic vessels, documented the vertebral occlusion. Chiropractic manipulation, which is increasing in popularity, may be a cause of potentially devastating neurologic disease.
A persistent trigeminal artery (PTA) represents an embryonic vascular anastomosis connecting the carotid and basilar arterial systems. Little is known about its protective role in cases of basilar artery occlusion. We followed up a 63-year-old man who had suffered a brain stem infarction due to basilar artery stenosis and was found to have a PTA. Although a second brain stem infarction due to basilar artery occlusion developed, the circulation to the brain stem was well maintained via collateral flow from the PTA, and the patient demonstrated good recovery. A PTA may function as an anastomosis between the carotid and basilar systems, thus preventing a more serious infarction.
A 43-year-old male with a left hemiparesis due to brain-stem infarction associated with bilateral persistent trigeminal arteries is reported. The clinicopathological and radiographic significance of persistent carotid-basilar arterial anastomoses in vertebrobasilar territory ischaemic attacks is also discussed.
The study case was a 66-year-old man who had bilateral neurosensory hearing impairment due to brain stem infarctions. He noticed mild hearing loss, frequent vertigo and tinnitus. About one month later, his hearing took a sudden turn for the worse, and he suffered from dysarthria, dysphagea and abasia. Neurological examination revealed pseudobulber palsy, left hemiparesis, cerebeller ataxia, disturbance of pain and temperature sensation on the right face and left side of the body. Brain stem auditory evoked potentials (BAEPs) showed a delayed small wave V with the abscence of previous waves on the right side and no significant waves on the left side. Brain magnetic resonance images (MRI) revealed infarctions in the bilateral middle cerebellar peduncles, including in the right lateral portions of pons, and the right lower pontine base. We believe that not only peripheral, but also central auditory pathways adjacent to infarctions were damaged. Magnetic resonance angiography (MRA) showed severe stenosis or occlusion of left vertebral artery and basilar artery. We concluded that hypoperfusion of the vertebrobasilar artery territories caused ischemia of the cochlear nerve and the auditory tracts in the brain stem, which resulted in bilateral hearing loss.
A 30 year old man admitted with a brain stem infarct presented with intellectual deterioration. A diagnosis of systemic lupus erythematosus (S.L.E.) was based on the presence of five A.R.A. criteria :photosensitivity, arthralgia, leukopenia and thrombopenia, false positive syphilitic serology, antinuclear factors on immunofluorescence. A lupus type circulating anticoagulant (L.C.A.) was no longer detected after corticotherapy. This appears to be a case of the "hematologic" form of S.L.E. in which the presence of L.C.A. predisposes towards thrombosis, not only of veins--which is typical--but also of arteries. These may be isolated and reveal the underlying disease as in the present case. The L.C.A. is an antibody possessing antiphospholipid specificity which explains the anticoagulant action in vitro and the thrombogenic effect in vivo. Some authors consider this to be sufficient justification for administration of anticoagulants and/or antiplatelet agents, but corticotherapy may be effective.
BACKGROUND AND PURPOSE: diffusion weighted magnetic resonance imaging (MRI) is highly sensitive in detecting acute supratentorial cerebral ischemia and Diffusion Weighted Imaging (DWI) lesion size has been shown to correlate strongly with the neurologic deficit in middle cerebral artery territory stroke. However, data concerning infratentorial strokes are rare. We examined the size and evolution of acute brain stem ischemic lesions and their relationship to neurological outcome. METHODS: brain stem infarctions of 11 patients were analyzed. We performed DWI in all patients and in 7/11 patients within 24 h, T2W sequences within the first 2 weeks (10/11 patients) and follow-up MRI (MR2) within 3-9 months (median 4.8 months) later (12/12 patients). Lesion volumes were compared with early and follow-up neurologic deficit as determined by National Institutes of Health Stroke Scale (NIHSS) score. RESULTS: the relative infarct volumes--with MR2 lesion size set to 100%--decreased over the time (P<0.02) with a mean shrinking factor of 3.3 between DWI (MR0) and the follow-up MRT (P<0.02), and 1.6 between early T2W (MR1) and MR2 (P<0.04). The mean DWI volume size (MR0) was larger than the early T2W (P<0.02). Although neurological outcome was good in all patients (mean NIHSS score of 1.3 at follow-up), early NIHSS and follow-up NIHSS scores were strongly correlated (r=0.9, P<0.00). NIHSS score at follow-up was highly correlated with lesion size of DWI (MR0; r=0.71, P<0.04) and T2W of MR1 (r=0.86, P<0.001). CONCLUSIONS: in this study, we saw a shrinking of the brain stem infarct volume according to clinical improvement of patients. Great extension of restricted diffusion in the acute stage does not necessarily implicate a large resulting infarction or a bad clinical outcome.
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Basilar and right vertebral artery occlusion, which caused a brain stem infarction, occurred in an 11-year-old boy. There have been nine previous cases of basilar artery occlusion with steno-occlusive lesion in the vertebral artery. It is suspected that dissection of the vertebral artery at the atlantoaxial level and a gradual progression of arterial dissection to the basilar artery were the major causes of this infarction.
We reported a 49-year-old male with brain stem infarction who had bilateral hearing impairment and tinnitus at the onset and subsequently developed various neurological symptoms, including bilateral lateral inferior pontine syndrome, one and a half syndrome and upward gaze palsy. Although CT scan failed to reveal any abnormalities initially, MRI revealed symmetrical foci bilaterally from the lateral inferior pons to the middle cerebellar peduncle, as well as in the paramedian portion of the mid-pons. Cerebral angiography: The left vertebral artery (VA) occluded at the 4th segment. The right VA showed severe stenosis at the 4th segment. The basilar artery (BA) was found to be occluded in the lower 1/3 below the clivus. Furthermore, CAG demonstrated upper portion of the BA, bilateral superior cerebellar artery and posterior cerebral artery via the posterior communicating artery, but the bilateral anterior inferior cerebellar arteries (AICAs) were absent or occluded. Neuroradiological findings suggested ischemia in the bilateral AICA and the middle portion of the BA. Bilateral hearing impairment rarely accompanies cerebrovascular disorders. This case of bilateral hearing impairment, tinnitus at the onset, followed by bilateral lateral inferior pontine syndrome was considered to be an extremely rare pathological condition.
Due to the great variety of clinical classification systems and syndromes, a representative overview of the etiology and prognosis of brain stem infarctions is missing. From the German Stroke Data Bank we therefore investigated 455 patients with visible brainstem infarction on cerebral imaging in comparison to patients with other infarct localizations. Follow-up after 3 and 12 months assessed functional outcome and recurrence of cerebral ischemia. Of 455 patients with acute brainstem infarction, 115 had additional infarctions in other vascular territories. In the remaining 340 patients with isolated brainstem infarction, the classification was: small vessel disease in 36.2%, macroangiopathy in 22.6%, and cardioembolism in 11.2%. After 3 months, 10% of the patients with isolated brainstem infarction had died and 55.6% were functionally independent. Mortality was 43.5% in patients with combined brainstem infarction. Our study highlights the frequency of small vessel disease as well as the relatively favorable prognosis in isolated brainstem infarction and preserved consciousness.
The authors report a case of superficial temporal to superior cerebellar artery anastomosis (STA-SCA anastomosis) for progressing rostral brain stem infarction with an excellent result. Precise operative techniques were also described. A 47-year-old male was admitted to our hospital on November 9, 1984, because of sudden onset of dysarthria and ataxic gait. CT revealed a low density area in the pons. Left vertebral angiogram showed occlusion of the left vertebral artery just distal to the origin of the posterior inferior cerebellar artery (PICA). Arterial branch of the left cerebellar hemisphere were filled via the left PICA to the left SCA and anterior inferior cerebellar artery anastomosis. Right brachial angiogram showed the hypoplastic right vertebral artery which ended at the PICA. The rostral basilar artery, both posterior cerebral arteries (PCA's) and right SCA were filled through anastomosis from the right PICA. The posterior circulation was not filled by either of the carotid arteries. In spite of antiplatelet agglutination therapy, the patient had two more episodes of dysarthria, dysphagia, right hemiparesis and gait disturbance. Because of progressing stroke, STA-SCA anastomosis was carried out on the right side on February 27, 1985. During operation, the blood pressure was maintained above the level of 130 mmHg, and intravenous mannitol injection and spinal drainage were done to preserve the right temporal lobe from intracerebral hematoma and/or edema caused by retraction. Postoperatively, the patient has been free from new ischemic attack. He has only slight hemiparesis now eight months after operation. Right external carotid angiogram showed a patent STA-SCA bypass and good filling of SCA's and PCA's bilaterally.(ABSTRACT TRUNCATED AT 250 WORDS)
A 35-year-old woman displayed unusual symptoms of progressive bulbar dysfunction. At necropsy, systemic necrotizing vasculitis and small pontine infarcts were demonstrated. The angiographic and magnetic resonance imaging findings are described. The latter investigation is a sensitive method for detecting such pontine lesions. To our knowledge, this case is the first report of magnetic resonance imaging findings of brain stem infarct in a patient with periarteritis nodosa.